ArticleFunctional & integrative genomics2024
GPC2 promotes prostate cancer progression via MDK-mediated activation of PI3K/AKT signaling pathway.
Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Proteoglycans in Prostate Cancer Progression and Therapy Resistance.Medicina (Kaunas, Lithuania) · 2025Review
- Significance of Midkine Signaling in Women's Cancers: Novel Biomarker and Therapeutic Target.International journal of molecular sciences · 2025Review
- Multiscale screening and identifying specific targets for artesunate in suppressing bladder cancer.Frontiers in pharmacology · 2025Article
- Identification of the gene signatures related to NK/T cell communication to evaluate the tumor microenvironment and prognostic outcomes of patients with prostate adenocarcinoma.Frontiers in immunology · 2025Article
- Integrative single-cell and spatial transcriptomics analysis reveals MDK-NCL pathway's role in shaping the immunosuppressive environment of lung adenocarcinoma.Frontiers in immunology · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
Prostate cancer is a major medical problem for men worldwide. Advanced prostate cancer is currently incurable. Recently, much attention was paid to the role of GPC2 in the field of oncology. Nevertheless, there have been no investigations of GPC2 and its regulatory mechanism in prostate cancer. Here, we revealed a novel action of GPC2 and a tumor promoting mechanism in prostate cancer. GPC2 was upregulated in prostate cancer tissues and cell lines. Higher expression of GPC2 was correlated with higher Gleason score, lymphatic metastasis, and worse overall survival in prostate cancer patients. Decreased expression of GPC2 inhibited cell proliferation, migration, and invasion in prostate cancer, whereas GPC2 overexpression promoted these properties. Mechanistically, GPC2 promoted the activation of PI3K/AKT signaling pathway through MDK. The rescue assay results in prostate cancer cells demonstrated that overexpression of MDK could attenuate GPC2 knockdown induced inactivation of PI3K/AKT signaling and partly reverse GPC2 knockdown induced inhibition of cell proliferation, migration, and invasion. In all, our study identified GPC2 as an oncogene in prostate cancer. GPC2 promoted prostate cancer cell proliferation, migration, and invasion via MDK-mediated activation of PI3K/AKT signaling pathway. GPC2 might be a promising prognosis predictor and potential therapeutic target in prostate cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.